The Kemp lab integrates intracellular signaling and metabolism in bioengineering studies of cellular immunity, toward the goal of targeted therapeutics for immunological diseases and cancer. Using a combination of computational and experimental methods, we investigate cytokine responses in T cells from a quantitative systems perspective. CD4+ helper T-cells produce interleukin-2 (IL-2) after ligand:receptor binding in order to activate other cells in an immune response. Increasing evidence linking chronic inflammation (a consequence of T helper cell activation) with cancer in multiple cell types highlights the need to pursue the mechanisms of T-cell activation as an avenue of cancer research. Observed changes in free radicals associated with T cell activation suggest that reactive oxygen species (ROS) play an important role in conveying receptor-ligation cues from the extracellular environment into an immune response. An understanding of the quantitative balance between signal transduction and oxidative state would provide insights into altering chemotherapy-resistant cancerous cells and enhancing the immune response for desensitized T cells in disease states.